Monthly Archives: September 2010

Lead V1 directly faces the right ventricle and during an inferior AMI may exhibit ST elevation with concomitant right ventricular infarction. Lead V1 also faces the endocardial surface of the posterolateral left ventricle, and ST depression may reflect concomitant posterolateral infarction (as the “mirror image” of ST elevation involving posterolateral epicardial leads). In this situation, V3 also shows ST depression. In lead V1, however, ST elevation from right ventricular AMI may potentially cancel out the ST depression from posterolateral AMI to give an isoelectric ST level. Diagnosis of right ventricular infarction during an inferior AMI may therefore be aided by evaluating both V1 and V3 ST levels. Both right ventricular infarction and postero-lateral infarction worsen the prognosis of an inferior AMI.

In 7967 patients with acute inferior myocardial infarction in the Hirulog and Early Reperfusion or Occlusion-2 (HERO-2) trial, V1 ST levels were analyzed with adjustment for lead V3 ST level for predicting 30-day mortality.

The authors conclude that V1 ST elevation identifies patients with acute inferior myocardial infarction who are at higher risk, although because no myocardial imaging was performed, could only speculate that the mechanistic link between V1 elevation and increased mortality is due to the occurrence of right ventricular infarction.

This is important to know about in terms of prognostication, but is it useful in the diagnosis of right ventricular AMI? The authors acknowledge that the ECG diagnosis of right ventricular infarction is classically made by recording lead V4R. In an autopsy study of 43 patients, ST elevation in lead V4R had higher sensitivity and specificity than ST elevation in lead V1 in diagnosing right ventricular infarction. Similarly, ST elevation in leads V7 through V9 adds significantly to precordial ST depression in aiding the diagnosis of posterolateral AMI. The authors contend that recording leads V4R and V7 through V9 is an additional step in the performance of a standard 12-lead ECG and, although recommended, may not be routinely performed.

I will continue to do a V4R in all inferior AMIs, and a V7-8 at least in patients with ST depression in V1-3.

A few years ago in the Emergency Department I managed a sick hypotensive, hypoxic 20-something year old with a unilateral lung white-out and air bronchograms as pneumonia/septic shock. He died subsequently of refractory pulmonary oedema on the ICU, where the diagnosis of acute pulmonary oedema due to severe aortic stenosis was delayed. Post mortem findings showed pulmonary oedema but no pneumonia. A kind radiologist told me the chest x-ray would certainly have fitted with pneumonia. After this case I learned to echo sick hypotensive patients in the ED.

Circulation reports 869 cardiogenic pulmonary oedema patients, of which 2.1% had unilateral pulmonary oedema (UPE). In patients with UPE, blood pressure was significantly lower (P<=0.01), whereas noninvasive or invasive ventilation and catecholamines were used more frequently (P=0.0004 and P<0.0001, respectively). The prevalence of severe mitral regurgitation in patients with bilateral pulmonary edema and UPE was 6% and 100%, respectively (P<0.0001). In patients with UPE, use of antibiotic therapy and delay in treatment were significantly higher (P<0.0001 and P=0.003, respectively). In-hospital mortality was 9%: 39% for UPE versus 8% for bilateral pulmonary edema (odds ratio, 6.9; 95% confidence interval, 2.6 to 18; P<0.001). In multivariate analysis, unilateral location of pulmonary edema was independently related to death.

Got a favourite assessment tool for classifying the severity of community acquired pneumonia? Two systematic reviews showed no significant differences in performance between Pneumonia Severity Index (PSI) and various versions of CURB (CURB, CURB-65, and CRB-65).
An accompanying editorial* opines that CRB-65 is the simplest tool and can easily be remembered. It also discusses some of the more subtle strengths and weaknesses of the tools.

A thought provoking article in Critical Care Medicine outlines basic science, animal, and human studies that suggest oestrogen may have a protective effect in a wide range of critical illnesses from cardiac arrest to trauma to stroke. It urges clinical trials of sex hormones, some of which are underway. Regarding traumatic brain injury, the authors state: “To date, studied interventions to treat the effects of secondary injury, such as induced hypothermia or sedative-hypnotic coma, have had disappointing results… Clearly, EMS (or emergency department) infusion of a single IV bolus of estrogen, a therapy shown in the laboratory to be a strong, direct, easy-to-deliver antioxidant, antiapoptotic, and anti-inflammatory intervention, has a much better chance of decreasing the severity of injury.“
Bold? Let’s see if studies such as this one show this intervention to be so beneficial.

Applying best evidence using simple easily remembered tools appeals to my small and busy brain. A system of minimising the impact of intensive care on long term brain function is proposed using an ABCDE mnemonic: awakening, spontaneous breathing trials, coordinating these two with target-based sedation, delirium monitoring and scoring, and early mobility therapy / exercise.

Being human, I suffer from confirmation bias: I’ve become aware that I’m always on the look out for studies that show benefit from physician-provided pre-hospital care and therefore it’s possible I miss the ones that show no benefit. Of course, no ‘level 1’ evidence is out there yet. This study isn’t hugely impressive, but worth adding to the list. After adjusting for injury severity, trauma patients treated on scene by Dutch physicians had no difference in mortality compared with those that received standard care. In the subgroup analysis for patients with severe traumatic brain injury, the mortality rate with physician involvement was lower than that without, but was not statistically significant. On scene times averaged 2.7 minutes longer in the physician group although factors that might have contributed to this, such as entrapment or on scene interventions, were not recorded.A Dutch Doctor
A major limitation in study design is that patients who died while under care at the scene or during transport were excluded from the analysis. The on scene time in these patients could have been prolonged by medical interventions in the field possibly contributing to the adverse outcome.
Take home message? More evidence needed.

A small randomised trial of adult emergency department patients showed faster insertion and higher success rates with the EZ-IO compared with the Bone Injection Gun (B.I.G). This is in keeping with my own experience and that of several services I have worked for.

EZ-IO

Bone Injection Gun

Comparison of two intraosseous access devices in adult patients under resuscitation in the emergency department: A prospective, randomized study Resuscitation. 2010 Aug;81(8):994-9

Okay – I admit to loving this paper, partly because it blows away the dogma of short scene times and ‘scoop & run’, and the oft-quoted but obnoxious assertion that the only pre-hospital fluid of benefit is gasoline.
A massive database of 3656 sick trauma patients (SBP < 90, 10>resp rate>29, GCS≤12, or advanced airway intervention), transported by 146 EMS agencies to 51 hospitals, was analysed to identify any association between mortality and emergency medical services (EMS) timings (activation, response, on-scene, transport, and total time). Overall mortality in this group was 22%.
There was no significant association between time and mortality for any EMS interval: activation (odds ratio [OR] 1.00; 95% confidence interval [CI] 0.95 to 1.05), response (OR 1.00; 95% CI 9.97 to 1.04), on-scene (OR 1.00; 95% CI 0.99 to 1.01), transport (OR 1.00; 95% CI 0.98 to 1.01), or total EMS time (OR 1.00; 95% CI 0.99 to 1.01).

The authors state: “In this study, we were unable to support the contention that shorter out-of-hospital times… improve survival among injured adults with field-based physiologic abnormality… Our findings are consistent with those of previous studies that similarly have failed to demonstrate a relationship between out-of-hospital time and outcome using different patient populations, trauma and EMS systems, regions, data sources, and confounders“

A trauma database was analysed to see if patients who were transported from the field to a non-trauma centre (NTC) and subsequently sent on to a trauma centre (TC) for definitive care fared worse than similar patients who were transferred directly to the TC.

There were 1,112 patients of whom 318 (29%) were initially triaged to a NTC. After adjusting for confounders, this was associated with an increase in prehospital crystalloids (4.2 L vs. 1.4 L, p < 0.05) and a 12-fold increase in blood transfusions (60% vs. 5%, p < 0.001). Age, injury severity score, Acute Physiology and Chronic Health Evaluation II score, and time from injury to TC arrival were independent predictors of mortality. The odds of death were 3.8 times greater (95% CI, 1.6–9.0) when patients were initially triaged to a nontrauma facility.

The authors conclude: triaging severely injured patients to hospitals that are incapable of providing definitive care is associated with increased mortality. Attempts at initial stabilization at an NTC may be harmful. These findings are consistent with a need for continued expansion of regional trauma systems.

One of the videos shows a nice demonstration of the McConnell sign (RV mid-segment dilation with apical sparing), which has been reported to be specific for (sub)massive PE. According to this article however, it has been reported that the McConnell sign is present in two thirds of patients with RV infarction and is only 33% specific for PE. Continuous wave Doppler helps differentiate RV infarction from submassive PE by demonstrating an increased tricuspid regurgitation RA-RV pressure gradient in submassive PE and a normal or low gradient in RV infarction.